聚（L—赖氨酸）盐酸与偶氮染料配合物诱导圆二色性的研究

本文探讨了聚(L-赖氨酸)盐酸与一组新型阴离子偶氮染料配合物的诱导圆二色性。从中发现对于同一类偶氮染料由于取代基不同(或分子的极性不同)其诱导旋光活性有较大变化,并利用激子手性方法确定了偶氮染料在配合物中的绝对构型.这对于研究生物高分子的生理作用提供了很有价值的资料。     

席夫碱型钯(II)配合物液晶的合成与表征

合成了带有端烯基的席夫碱型配体 (Schiff_C11C10 )及其含氯桥型的钯 (II)配合物 (Schiff_C11C10 _Pd) ,通过元素分析 ,摩尔电导 ,红外光谱 ,电子光谱 ,核磁共振等进行了表征 .配合物为中性配合物 ,配体与Pd(II)的摩尔比为 1∶1.配体和配合物均为热致型液晶 .配体和配合物介晶相皆为近晶相 ,配体的液晶态初步判定为镶嵌状织构 ,配合物的液晶态为破扇状织构 .     

Cu(Ⅱ),Co(Ⅱ),Ni(Ⅱ)与2,2'-二硫代二苯甲酸配合物的合成与表征

以2,2′-二硫代二苯甲酸为配体,分别与铜(Ⅱ)、钴(Ⅱ)、镍(Ⅱ)合成了三种过渡金属配合物,通过元素分析、ICP发射光谱和热重分析确定了配合物的组成;并用红外光谱、荧光光谱和热重分析进行了表征.结果表明:2,2′-二硫代二苯甲酸与与铜(Ⅱ)、钴(Ⅱ)、镍(Ⅱ)形成摩尔比为1∶1型配合物,三种配合物均具有较强的荧光性能,配合物热稳定性为:镍(Ⅱ)和钴(Ⅱ)高于铜(Ⅱ).     

Cu-PAR稳定常数的配体竞争-等色点光度法测定

本文研究了“配体竞争一等色点光度法”测定高稳定性配合物的稳定常数,利用该法研究铜(Ⅱ)与PRA的配位反应,测得该反应生成1:1型配合物1gK_(ML)=16.44,1:2型配合物1gK_(m12)=25.93。     

双吡啶吡咯Cu(Ⅱ)配合物与DNA相互作用研究

合成了1种单核双吡啶吡咯Cu(Ⅱ)配合物[Cu(PDPH)2] (1),其中配体HPDPH为2,5-二(2′-吡啶基)吡咯.该配合物晶体属于单斜晶系,空间群为C2/c,a＝39.1242(16) ?,b＝8.6574(5) ?,c＝33.7687(14) ?,β＝123.0305(16)°,中心离子Cu2＋处于变形八面体配位环境.采用紫外-可见光谱、荧光光谱及圆二色谱等方法,分别研究了单核配合物[Cu(PDPH)2] (1)、双核配合物[Cu2(PDPH)2(NO3)2] (2)和多聚配合物{[Cu2(PDPH)2(N3)2]}n(3)与DNA之间的相互作用.结果表明,3个Cu(Ⅱ)配合物均以沟面键合方式与CT-DNA结合,其结合强弱顺序为3 > 2 > 1.此外,采用凝胶电泳法研究了3种Cu(Ⅱ)配合物对超螺旋pBR322 DNA的切割作用.结果表明,3种配合物均能将pBR322 DNA切割为开口缺刻型或者线型DNA,表现出良好的切割活性.     

香草醛缩多胺Schiff碱Ou（Ⅱ）配合物的固相合成、表征及其稳定性和抑菌活性

为Schiff碱Cu(Ⅱ)配合物稳定性与抑菌活性之间的关系提供理论和实验上的依据,以香草醛为原料,分别与乙二胺、二乙烯三胺、三乙烯四胺合成3种Schiff碱配体L1,L2和L3,在室温下与醋酸铜进行固相合成,得到3种新的Schiff碱Cu(Ⅱ)配合物。通过元素分析、红外光谱(IR)、热重(TG-DTA)、分光光度法等测试手段进行了表征。在400nm工作波长下,测定配合物的稳定常数,分别为1.24×104、0.93×104和0.71×104,结果表明:Cu(Ⅱ)与配体L1,L2和L3之间分别形成了1∶1,1∶2和1∶2型配合物,且配合物的稳定性随配体中R基的增大而减小。对Schiff碱配体及其相应配合物进行了抑菌活性实验,结果表明:配体和Cu(Ⅱ)配合物对大肠杆菌、枯草杆菌和八叠球菌均有一定的抑制作用,而且配合物比相应配体的抑菌活性强,配合物稳定性越强,其抑菌活性越强。     

类Friedel-Crafts酰基化合成苯基二氯化膦中催化剂AlCl_3的催化与失活机理探究

苯和PCl_3在无水AlCl_3作用下发生类Friedel-Crafts酰基化反应,生成主产物苯基二氯化膦(dichlorophenylphosphine,BPD)和副产物二苯基氯化膦(chlorodiphenylphosphine,DPC),反应中AlCl_3可分别与PCl_3、BPD、DPC形成配合物,而且配合物的稳定性和配位方式对此催化反应起着重要作用。以PCl_3-AlCl_3(1)、BPD-AlCl_3(2)和DPC-AlCl_3(3)配合物为研究对象,采用量子化学计算方法对三种配合物的配位方式和两单体分子之间的相互作用能进行研究。结果表明:AlCl_3与PCl_3、BPD、DPC均可能有两种配位类型,AlCl_3中的Al原子与配体中的Cl原子配位形成A型配合物,AlCl_3中的Al原子与配体中的P原子配位形成B型配位物;A型配合物可形成明显的P+区域,有利于进一步的亲电取代反应,其中A-1(A型PCl_3-AlCl_3)和A-2(A型BPD-AlCl_3)的P+区域进攻苯环分别生成BPD和DPC;B型配合物中的P—Al键的共价成分较A型配合物中的Cl—Al键的共价成分高;两种配合物都符合PCl_3-AlCl_3、BPD-AlCl_3、DPC-AlCl_3相互作用强度依次增大的规律,因此配合物在体系中解离出AlCl_3越来越困难,进而导致催化剂不断失活。     

吡啶-2,6-双酰胺镉(Ⅱ)配合物的合成与表征

利用水热法合成了3种吡啶-2,6-双酰胺分子吡啶-2,6-二[N-(1'-羟乙基)甲酰胺]、吡啶-2,6-二[N-(2'-羟丙基)甲酰胺]、吡啶-2,6-二[N-(1',1'-二甲基-2'-羟基)甲酰胺]的镉(Ⅱ)配合物,通过元素分析方法确定配合物的组成,比较分析配位前后游离配体与配合物的红外和紫外吸收光谱,推测了配合物的可能结构,并采用紫外光谱滴定法对配体与Cd(Ⅱ)离子在溶液中的配位行为进行了模拟研究。结果显示3种镉(Ⅱ)配合物的配位模式相同,均为1∶1 ML型,配体中两个酰胺键N原子和吡啶环N原子作为配位原子参与金属离子Cd(Ⅱ)配位成键。     

5-硝基水杨醛氨基酸Schiff-bases铜配合物与DNA相互作用的研究

用电子光谱、荧光淬灭光谱和循环伏安的方法,研究了(苯丙氨酸缩5-硝基水杨醛)铜(1)和(组氨酸缩5-硝基水杨醛)铜(2)与DNA的作用.结果表明,配合物均以插入模式与DNA作用;配合物与DNA作用强弱为:配合物(2)＞配合物(1).     

香草醛缩多胺Schiff碱Cu(Ⅱ)配合物的固相合成、表征及其稳定性和抑菌活性

为Schiff碱Cu(Ⅱ)配合物稳定性与抑菌活性之间的关系提供理论和实验上的依据,以香草醛为原料,分别与乙二胺、二乙烯三胺、三乙烯四胺合成3种Schiff碱配体L1,L2和L3,在室温下与醋酸铜进行固相合成,得到3种新的Schiff碱Cu(Ⅱ)配合物。通过元素分析、红外光谱(IR)、热重(TG-DTA)、分光光度法等测试手段进行了表征。在400nm工作波长下,测定配合物的稳定常数,分别为1.24×104、0.93×104和0.71×104,结果表明:Cu(Ⅱ)与配体L1,L2和L3之间分别形成了1∶1,1∶2和1∶2型配合物,且配合物的稳定性随配体中R基的增大而减小。对Schiff碱配体及其相应配合物进行了抑菌活性实验,结果表明:配体和Cu(Ⅱ)配合物对大肠杆菌、枯草杆菌和八叠球菌均有一定的抑制作用,而且配合物比相应配体的抑菌活性强,配合物稳定性越强,其抑菌活性越强。     

长吻(鱼危)幼鱼的生态效率初探

长吻鮠幼鱼的总平均生态效率为11.44%,饵料系数7.41;在适宜的温度范围内,随水温上升,幼鱼体重增加.生态效率增大.在24.9℃以上的适温范围内,幼鱼生长快;密度对幼鱼的生长有明显影响,适宜的放养密度,幼鱼生长快,在本试验条件下.最适密度是12尾/m~2.     

急性白血病T淋巴细胞及其亚群的研究

应用McAb检测31例急性白血病患者外周血T细胞及其亚群的改变。结果表明总T细胞(T_1)、T辅助细胞(T_4)和T抑制细胞(T_8)百分率均明显低于正常对照组(P<0.01～0.001),且伴有T_4:T_8值的下降(P<0.05)。经化疗缓解后,部分缓解组T细胞及其亚群均恢复正常,完全缓解组T_4细胞仍稍低于正常值(P<0.05)。化疗无效组T细胞及其亚群的改变与未治疗组类似(P>0.05)。急淋T-ALL型时,外周血T细胞及其亚群的改变与一般白血病表现不同,其T细胞标记及T_4:T_8值反而增高。病情缓解时逐渐恢复正常急淋其它型患者,其T细胞及亚群的改变与急非淋患者类似。结果提示,动态观察T细胞及其亚群变化,有助于对白血病患者疗效及预后的判定。     

PD-1 expression on HIV-specific T cells is associated with T-cell exhaustion and disease progression

Functional impairment of T cells is characteristic of many chronic mouse and human viral infections. The inhibitory receptor programmed death 1 (PD-1; also known as PDCD1), a negative regulator of activated T cells, is markedly upregulated on the surface of exhausted virus-specific CD8 T cells in mice. Blockade of this pathway using antibodies against the PD ligand 1 (PD-L1, also known as CD274) restores CD8 T-cell function and reduces viral load. To investigate the role of PD-1 in a chronic human viral infection, we examined PD-1 expression on human immunodeficiency virus (HIV)-specific CD8 T cells in 71 clade-C-infected people who were naive to anti-HIV treatments, using ten major histocompatibility complex (MHC) class I tetramers specific for frequently targeted epitopes. Here we report that PD-1 is significantly upregulated on these cells, and expression correlates with impaired HIV-specific CD8 T-cell function as well as predictors of disease progression: positively with plasma viral load and inversely with CD4 T-cell count. PD-1 expression on CD4 T cells likewise showed a positive correlation with viral load and an inverse correlation with CD4 T-cell count, and blockade of the pathway augmented HIV-specific CD4 and CD8 T-cell function. These data indicate that the immunoregulatory PD-1/PD-L1 pathway is operative during a persistent viral infection in humans, and define a reversible defect in HIV-specific T-cell function. Moreover, this pathway of reversible T-cell impairment provides a potential target for enhancing the function of exhausted T cells in chronic HIV infection.     

Recognition of cluster of differentiation 1 antigens by human CD4-CD8-cytolytic T lymphocytes

Human cluster-of-differentiation 1 (CD1) is a family of cell surface glycoproteins of unknown function expressed on immature thymocytes, epidermal Langerhans cells and a subset of B lymphocytes. Three homologous proteins, CD1a, b and c, have been defined serologically, and the CD1 gene locus on human chromosome 1 contains five potential CD1 genes. Analysis of the predicted amino-acid sequences of CD1 molecules reveals a low but significant level of homology to major histocompatibility complex (MHC) class I and class II molecules, and, like MHC class I molecules, CD1 molecules are associated non-covalently with beta 2-microglobulin. These structural similarities to known antigen-presenting molecules, together with the expression of CD1 on cells capable of antigen presentation, suggest a role for CD1 molecules in antigen recognition by T cells. Here we demonstrate the specific recognition of CD1a by a CD4-CD8- alpha beta T-cell receptor (TCR) expressing cytolytic T lymphocyte (CTL) line and the specific recognition of CD1c by a CD4-CD8- gamma delta TCR CTL line. The interaction of CD1-specific CTLs with CD1+ target cells appeared to involve the CD3-TCR complex, and did not show evidence of MHC restriction. These results suggest that for a subset of T cells, CD1 molecules serve a function analogous to that of MHC class I and II molecules.     

大鼠肝窦内皮细胞的分离、鉴定及纯度、活性分析

按Higgins等方法制作大鼠2／3肝切除（parital hepatectomy,PH）模型,用两步灌流法分散肝脏细胞,用60％ Percoll梯度离心和免疫磁珠分离肝窦内皮细胞（hepatic sinusoidal endothelial cell,SEC）,用分化抗原簇14（cluster of differentiation 14,CD14）和内皮素-1（endothelin-1,ET-1）的免疫组织化学定性、定位再生肝（regenerating liver,RL）、分散的肝脏细胞及分离的窦内皮细胞,用RT—PCR定量窦内皮细胞的CDl1和ET-1的mRNA,用蛋白免疫印迹方法定量窦内皮细胞的CD14和ET-1蛋白．初步证实,分离的窦内皮细胞中CD14和ET-1阳性细胞占95％以上,从PH后各时间点分离的窦内皮细胞的CD14和ET-1mRNA量稳定,相应的蛋白量亦稳定．表明改进的分离窦内皮细胞方法具有收率和纯度高、活性好等特点,值得采用．     

v-Fos transformation effector binds with CD2 cytoplasmic tail

The CD2 molecule, an adhesive and co-stimulating molecule, expresses virtually on all T lymphocytes, thymocytes, as well as natural killer cells, playing an important role in thymus development, T cell activation and apoptosis[1―3]. CD2 molecule consists of an ex- tracellular region with two Ig-like domains, a single membrane-spanning domain, and a positively charged proline-rich cytoplasmic tail, which is highly conserved between different species[1,4―7]. The functions of CD2 in signal t…     

直接免疫荧光法分析白血病及骨髓增生异常综合征患者免疫表型

目的 :检测急性白血病 (AL)及骨髓增生异常综合征 (MDS)免疫表型及其临床意义。方法 :用流式细胞仪CD4 5设门直接免疫三标记法 ,检测 4 9例AL及MDS患者免疫表型。结果 :ALL双克隆型 9例 ,其中髓系伴T -ALL 3例 ,髓系伴B -ALL 4例 ,1例为髓系伴T、B标记 (CD13 +CD7+CD19+ ) ,1例同时CD7+CD19+ ;ALL同时表达CD3 4 及HLA -DR最高 (6 0 .0 1%) ,明显高于AML、MDS(P <0 .0 0 5 )。AML双克隆型 2 0例 ,7例为髓系伴CD7+ ,2例髓系伴CD19+ ,11例为同时表达CD3 4 +HLA -DR +。MDS患者骨髓细胞表达髓系成熟抗原CD13 +及CD3 3 +增高 ,未发现淋系抗原的表达。MDS -RAEB、RAEBT及转为白血病病例均高表达CD3 4 及HLA -DR抗原。结论 :用三标记法简便易行 ,提高诊断准确性 ;单抗组合应兼顾髓、淋系同时表达 ;应加胞浆抗原检测。     

CD1b restricts the response of human CD4-8- T lymphocytes to a microbial antigen.

Molecules encoded by the human CD1 locus on chromosome 1 (ref. 33) are recognized by selected CD4-8- T-cell clones expressing either alpha beta or gamma delta T-cell antigen receptors. The known structural resemblance of CD1 molecules to antigen-presenting molecules encoded by major histocompatibility complex (MHC) genes on human chromosome 6 (refs 3, 4, 34, 35), suggested that CD1 may represent a family of antigen-presenting molecules separate from those encoded in the MHC. Here we report that the proliferative and cytotoxic responses of human CD4-8- alpha beta TCR+ T cells specific for Mycobacterium tuberculosis can be restricted by CD1b, one of the four identified protein products of the CD1 locus. The responses of these T cells to M. tuberculosis seemed not to involve MHC encoded molecules, but were absolutely dependent on the expression of CD1b by the antigen-presenting cell and involved an antigen processing requirement similar to that seen in MHC class II-restricted antigen presentation. These results provide, to our knowledge, the first direct evidence for the proposed antigen-presenting function of CD1 molecules and suggest that the CD1 family plays a role in cell-mediated immunity to microbial pathogens.     

程序光盘目录结构剖析

为了解决用户直接读取程序光盘文件的问题及掌握程序光盘目录结构 ,本文对程序光盘目录结构进行了详尽的剖析 .并给出确定程序光盘、读取程序光盘相关目录结构、目录文件结构的方法     

CD69 acts downstream of interferon-alpha/beta to inhibit S1P1 and lymphocyte egress from lymphoid organs

Naive lymphocytes continually enter and exit lymphoid organs in a recirculation process that is essential for immune surveillance. During immune responses, the egress process can be shut down transiently. When this occurs locally it increases lymphocyte numbers in the responding lymphoid organ; when it occurs systemically it can lead to immunosuppression as a result of the depletion of recirculating lymphocytes. Several mediators of the innate immune system are known to cause shutdown, including interferon alpha/beta (IFN-alpha/beta) and tumour necrosis factor, but the mechanism has been unclear. Here we show that treatment with the IFN-alpha/beta inducer polyinosine polycytidylic acid (hereafter 'poly(I:C)') inhibited egress by a mechanism that was partly lymphocyte-intrinsic. The transmembrane C-type lectin CD69 was rapidly induced and CD69-/- cells were poorly retained in lymphoid tissues after treatment with poly(I:C) or infection with lymphocytic choriomeningitis virus. Lymphocyte egress requires sphingosine 1-phosphate receptor-1 (S1P1), and IFN-alpha/beta was found to inhibit lymphocyte responsiveness to S1P. By contrast, CD69-/- cells retained S1P1 function after exposure to IFN-alpha/beta. In coexpression experiments, CD69 inhibited S1P1 chemotactic function and led to downmodulation of S1P1. In a reporter assay, S1P1 crosslinking led to co-crosslinking and activation of a CD69-CD3zeta chimaera. CD69 co-immunoprecipitated with S1P1 but not the related receptor, S1P3. These observations indicate that CD69 forms a complex with and negatively regulates S1P1 and that it functions downstream of IFN-alpha/beta, and possibly other activating stimuli, to promote lymphocyte retention in lymphoid organs.